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34-year old male patient recently diagnosed with AIDS (Cellular Immune…
34-year old male patient recently diagnosed with AIDS
Unprotected sex
Sharing needles
HIV will never go away, even if AIDS never develops.
AIDS is the late stage HIV infection.
HIV attacks the body’s immune system (T cells)
Help the immune system fight off infections
Harder for the body to fight off other infections
Minor infection can be much more severe
If left untreated, HIV can lead AIDS
HIV: Immediate effects on the body
Usually appear after 2-6 weeks
Fever
Skin rash
Sore throat
Swollen glands
Joint or muscle pain
Effects of medication
Headache
Tiredness
Diarrhea
Nausea or vomiting
Rash
High blood sugar levels
High cholesterol
AIDS
The number of CD4 cells falls below 200 cells per cubic millimeter of blood (200 cells/mm3)
In a healthy immune system
CD4 counts are between 500 and 1,600 cells/mm3.
Develop one or more opportunistic infections regardless of CD4 count.
Herpes simplex virus 1 (HSV-1) infection
Toxoplasmosis
Candidiasis
Salmonella infection
Without ART people with AIDS typically survive about 3 years
Life expectancy without treatment falls to about 1 year
Starting ART soon after get HIV testing experience more benefits
Antiretroviral therapy or ART
Combination of antiretroviral drugs to maximally suppress HIV.
ART also prevents onward transmission of HIV.
The difference between HIV and AIDS
human immunodeficiency virus
Virus
can lead to immune system deterioration
Attacks the immune system
Acquired immunodeficiency syndrome
HIV can lead to the development of AIDS.
Stage 3 HIV
Condition
Immune system
Resistance to disease
Innate (nonspecific) defense system
Constitutes first and second lines of defense
Adaptive (specific) defense system
Third line of defense attacks particular foreign substances
First Line of Defense
Skin and mucous membranes
produce protective chemicals that inhibit or destroy microorganisms
Acid
Enzymes
Mucin
Defensins
Respiratory system also has modifications to stop pathogens
Second Line of Defense
Phagocytes
Neutrophils
Use Defensins to pierce membrane of pathogen
Macrophages
Develop from monocytes and are chief phagocytic cells
Natural killer (NK) cells
Large granular lymphocytes that police blood and lymph
Can kill cancer and virus-infected cells before adaptive immune system is activated
The foreign or infected cell goes through apoptosis
Inflammatory response
Antimicrobial proteins
Fever
Leukocytes and macrophages exposed to foreign substances secrete pyrogens
Pyrogens act on body’s thermostat in hypothalamus
Antimicrobial Proteins
Attack microorganisms directly
Hinder microorganisms’ ability to reproduce
Interferons
Proteins produced by lymphocytes or “infected” cells
“Warns” healthy neighboring cells (especially viral)
activate NK cells and macrophages
Complement
Plasma proteins that circulate in blood in inactive form
Provides major mechanism for destroying foreign substances
Activation enhances inflammation and also directly destroys bacteria
Pathway
Antibodies bind to invading organisms and then bind to complement components (activating them)
Alternate pathway does not require antibody to be activated
tags a pathogen (opsonization)
calls upon phagocytic cells
pokes holes into pathogen
Adaptive Defenses
eliminates almost any pathogen or abnormal cell in body; T-cells and B-cells
Recognizes and targets specific antigens
Not restricted to initial site
Mounts an even stronger attack to “known” antigens (second and subsequent exposures)
Humoral (antibody-mediated) immunity
Antibodies, produced by B lymphocytes, circulate freely in body fluids
Temporarily inactivate (different ways-later)
Mark for destruction by phagocytes (or complement)
Cellular (cell-mediated) immunity
Lymphocytes act against target cell
Directly—by killing infected cells
Indirectly—by releasing chemicals that enhance inflammatory response; or activating other lymphocytes or macrophages
Antigens
foreign substances/molecules that can mobilize adaptive defenses and provoke an immune response
Characteristics
Complete antigen or hapten (incomplete)
Complete are large, immunogenic and reactive (reacts with the lymphocytes and any antibodies)
Antigenic determinants
Part of antigen that is stimulating the army creation
Haptens
Molecules too small to be seen so are not immunogenic by themselves
Becomes immunogenic if it attaches to body’s own proteins
Self-antigens
All cells are covered with variety of proteins located on surface
MHC proteins- A self-protein
Has a “groove” to hold piece of self-antigen or foreign antigen
T lymphocytes can recognize only antigens that are presented on MHC proteins
Lymphocytes
B lymphocytes (B cells)—humoral immunity- pathogens outside of cell
T lymphocytes (T cells)—cellular immunity- pathogens inside the cell
Lymphocyte development, maturation, and activation
Lymphocytes originate in red bone marrow
Maturation
“Educate” in a 2-3 days and mature in primary lymphoid organs (for 2 reasons)
Immunocompetence: must be able to recognize only 1 specific antigen
Have only one unique type of antigen receptor on surface when mature so bind only one specific antigen
Self-tolerance: lymphocytes must be unresponsive to own antigens
Education during Maturation
T cells mature in thymus under negative and positive selection pressures “tests”
Positive
Selects T cells capable of recognizing self-MHC proteins
Negative
Destruction of T cells that bind to self-antigens displayed by self-MHC
Seeding secondary lymphoid organs and circulation
B and T cells not yet exposed to antigen naïve (so can bind to antigen, but haven’t been fully activated yet)
Exported from primary lymphoid organs to colonize secondary lymphoid organs (Increases chance of encounter with antigen)
Antigen encounter and activation
Naive lymphocyte’s first encounter with antigen triggers lymphocyte to develop further differentiates into an active cell
Proliferation and differentiation
Lymphocyte proliferates, forms “army” of exact copies of itself, referred to as clones
Most clones become effector cells that fight infections
A few remain as memory cells
Able to respond to same antigen more quickly second time it is encountered
B and T memory cells and effector T cells circulate continuously
Antigen receptor diversity
Genes
determine which foreign substances the immune system will recognize
Antibodies
are proteins secreted by plasma cells
Make up gamma globulin portion of blood
Capable of binding specifically with antigen detected by B cells
IgM, IgA, IgD, IgG, and IgE
IgM
IgM
First antibody released
Potent agglutinating agent
Readily fixes and activates complement
IgA
Found in mucus and other secretions
Helps prevent entry of pathogens
IgG
75–85% of antibodies in plasma
Almost all secondary responses
IgE
Active in some allergies and parasitic infections
Causes mast cells and basophils to release histamine
do not destroy antigens; they inactivate
Neutralization
Antibodies block specific sites on viruses or
bacterial exotoxins
Prevent antigens from binding to receptors on tissue cells
Antigen-antibody complexes undergo phagocytosis
Agglutination
antigen-antibody complexes become cross-linked into large clumps
Precipitation
Antibodies bind with floating/unattached antigens- complexes precipitate out of solution
Precipated complexes eaten by phagocytes
Complement fixation
Main antibody defense against cellular antigens (bacteria, mismatched RBCs)
Cellular Immune Response
T cells provide defense against
cells infected with viruses or bacteria,
cancerous or abnormal cells,
foreign (transplanted) cells
Most T-cells “help” other cells by releasing cytokines
The antigen is usually presented to the T cell by a macrophage
Helper T cells
Through antigen binding or cytokines…
These cells can activate B cells, and other T helpers cells
inform other cells, like macrophages/dendritic, of a problem
Regulatory T cells
moderate immune response
Memory T cells
Cytotoxic T cells
killers; capable of destroying cells harboring foreign antigens
APCS
Engulf antigens and present fragments of antigens to T cells for recognition
Dendritic cells
Phagocytize pathogens in skin/mucous membranes
Then enter lymphatics to present antigens to T cells in lymph node
Macrophages
Phagocytize pathogens in connective tissues and lymphoid organs
Present antigens to T cells, which not only activates T cell, but also further activates macrophage
B lymphocytes
Present antigens to helper T-cell
provokes humoral immune response
effector cells quickly multiply
Most are plasma cells, and these make antibodies specific for that particular antigen
Secrete antibodies at rate of 2000 molecules per second for 4 to 5 days, then die
Antibodies circulate in blood or lymph, binding to free antigens, marking them for destruction by innate or other adaptive mechanisms
Active humoral immunity
Naturally acquired: formed in response to actual bacterial or viral infection
Artificially acquired: formed in response to vaccine
Occurs when B cells encounter antigens and produce specific antibodies against them
Passive humoral immunity
occurs when ready-made antibodies are introduced into body
Naturally acquired: antibodies delivered to fetus via placenta or to infant through milk
Artificially acquired: injection of serum, such as gamma globulin
B cells
Do not respond to specific antigens
Macrophages, Dendritic cells, B cells
Carry a piece of the antigen on themselves and “present” it